Study Of Angiogenesis In Esophageal And Gastric Tissue Of Patients With Portal Hypertension

Traditionally, formation of esophagogastric varices was considered to be a mechanical consequence of the increased portal pressure that will result in the opening of portal-systemic collateral vessels. However, these varicose veins increase not only in size but also in number. We hypothesized that the formation ot esophagogastric varices could also involve active angiogenesis. Vascular endothelial growth factor (VEGF) is a potent angiogenic factor involved in both physiological and pathological angiogenesis. And the expression of VEGF is potentiated in response to hypoxia. Portal hypertension causes the passive congestion and hypoxia of esophagogastric mucosal. Transjugular intrahepatic portosystemic shunt (TIPS) can decrease portal pressure, lighten esophagogastric varices and improve the circulation of esophageal and gastric tissue. In this study, we investigate the expression of vascular endothelial growth factor in esophageal and gastric tissue and microvessle density and its correlation with changes of portal pressure, and explore whether the angiogenesis contribute to the formation of esophagogastric varices in portal hypertension.Part one Expression of vascular endothelial growth factor in esophageal and gastric tissue of patients with portal hypertensionand changes after TIPSObjectiveTo investigate the expression of vascular endothelial growth factor (VEGF) inesophageal and gastric tissue and its correlation with changes of portal pressure, and explore the role of VEGF in the formation of esophagogastric varices in portal hypertension. MethodsSpecimens from portal hypertension patients underwent modified Sugiura procedure were divided into two groups. In PHT group, 18 cases of esophageal tissue and 25 cases of gastric tissue were taken from patients untreated with TIPS before operation. In TIPS group, 5 cases of esophageal tissue and 12 cases of gastric tissue were taken from patients treated with TIPS before operation. Normal esophageal tissue (10 cases) and gastric tissue (8 cases) served as the control group. The expression of VEGF in esophageal and gastric tissue was studied quantitatively by immunohistochemistry SP method and computer assisted image analysis system. ResultsThe expression of VEGF was mainly seen in the mucosal layer both in esophageal tissue and gastric tissue. There was no significance difference in positive region of VEGF among groups. Gray level of positive regions in either esophageal tissue or gastric tissue of the three groups was ranked as follows by statistical comparison: PHT group > TIPS group >control group (P<0.01) . That was the VEGF levels of the three groups lined as follows: PHT group > TIPS group > control group. ConclusionThe expression of VEGF in esophageal and gastric tissue is related with changes of portal pressure. The expression of VEGF increases in portal hypertension while decreases after TIPS. The increased expression of VEGF may contribute to the formation of esophagogastric varices in portal hypertension.Part two Changes of microvessle density in esophageal andgastric tissue of patients with portal hypertensionObjectiveTo investigate the changes of microvessle density in esophageal and gastric tissue of patients with portal hypertension.